Journal
NATURE REVIEWS NEUROSCIENCE
Volume 15, Issue 6, Pages 394-409Publisher
NATURE PUBLISHING GROUP
DOI: 10.1038/nrn3680
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Funding
- Biotechnology and Biological Sciences Research Council (BBSRC)
- Faculty of Medicine and Health Sciences, University of Nottingham, UK, non-clinical senior fellowship
- BBSRC [BBS/E/B/000C0417] Funding Source: UKRI
- Biotechnology and Biological Sciences Research Council [BBS/E/B/000C0417] Funding Source: researchfish
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Axon degeneration is a prominent early feature of most neurodegenerative disorders and can also be induced directly by nerve injury in a process known as Wallerian degeneration. The discovery of genetic mutations that delay Wallerian degeneration has provided insight into mechanisms underlying axon degeneration in disease. Rapid Wallerian degeneration requires the pro-degenerative molecules SARM1 and PHR1. Nicotinamide mononucleotide adenylyltransferase 2 (NMNAT2) is essential for axon growth and survival. Its loss from injured axons may activate Wallerian degeneration, whereas NMNAT overexpression rescues axons from degeneration. Here, we discuss the roles of these and other proposed regulators of Wallerian degeneration, new opportunities for understanding disease mechanisms and intriguing links between Wallerian degeneration, innate immunity, synaptic growth and cell death.
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